ArticleNeuron2018
TREM2 Is a Receptor for β-Amyloid that Mediates Microglial Function.
Open access · bronzeAbstract read
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Article in Neuron, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 453 papers.
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453citing papers in PubMed
33.2field-weighted citation impact, top 1% of its field
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Who cites it
453 citing papers in PubMed, 786 citations in OpenAlex.
- The TREM2 agonistic antibody AL002 in early Alzheimer's disease: a phase 2 randomized trial.Nature medicine · 2026Trial
- Plasma exchange with albumin replacement for Alzheimer's disease treatment induced changes in serum and cerebrospinal fluid inflammatory mediator levels.Annals of clinical and translational neurology · 2024Trial
- Preclinical and first-in-human evaluation of AL002, a novel TREM2 agonistic antibody for Alzheimer's disease.Alzheimer's research & therapy · 2024Trial
- TREM2 in glioma: Reprogramming the immune microenvironment from mechanistic understanding to clinical translation (Review).Molecular medicine reports · 2026Review
- The TREM2 R47H variant is associated with liver-plasma-brain axis dyshomeostasis in the 5xFAD mouse model of Alzheimer's disease.Neurobiology of aging · 2026Article
- Uncovering the biological mechanisms of TREM2 with molecular simulations: A comprehensive review and perspective.Progress in biophysics and molecular biology · 2026Review
- TMEM59 regulates microglial Aβ phagocytosis in a TREM2-dependent manner and acts as a potential therapeutic target for Aβ amyloidosis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Glycation at the Gate: A Brain Endothelial Glycocalyx Model and Therapeutic Roadmap for Alzheimer's Disease.Biomedicines · 2026Article
- DNA Sensing Pathways in Innate Immunity: Implications for Alzheimer's Disease Progression and Therapy.Molecular neurobiology · 2026Review
- Modeling stimulus-induced stress responses in microglia-like cells using a commercial iPSC-dCas9-KRAB line.Stem cell research · 2026Article
- The Glial Autophagy-Lysosomal-Inflammation Axis in Alzheimer's Disease: a Unifying Mechanistic Framework.Molecular neurobiology · 2026Review
- Targeting Mitochondrial Dysfunction in Microglia: A New Frontier for Treating Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- APOEε4 attenuates early TREM2-mediated microglial responses and influences disease trajectories in dementia with Lewy bodies.Research square · 2026Article
- TREM2 in neurodegenerative diseases and acute neurological injuries: mechanisms to targeted therapies.Cell communication and signaling : CCS · 2026Review
- Reshaping the immune landscape: next-generation microglia-targeted therapies for Alzheimer's disease.Biological research · 2026Review
- Cholesterol at the Center of Alzheimer's Disease: A Unifying Hypothesis on the Pathogenic Mechanism.Molecules (Basel, Switzerland) · 2026Review
- Microglia and neuroinflammation: function, heterogeneity, and crosstalk.Cellular & molecular immunology · 2026Review
- Increased circulating TREM2Brain, behavior, & immunity - health · 2026Article
- Peripheral and central immune features in insomnia: Integrative bulk and single-cell transcriptomic analyses reveal core hub genes and candidate compounds.Functional & integrative genomics · 2026Article
- Microglial ITAM & ITIM Signaling in Neurodegenerative Disease and Brain Aging.Journal of molecular biology · 2026Review
393 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 4 institutions in 2 countries.
Yingjun ZhaoNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Xilin WuNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA; Department of Neurology, Union Hospital, and Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, Fujian 350001, China.
Xiaoguang LiNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Lu-Lin JiangNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Xun GuiTexas Therapeutics Institute, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Yan LiuNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA; Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian 361102, China.
Yu SunNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Bing ZhuNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Juan C Piña-CrespoNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Muxian ZhangFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian 361102, China.
Ningyan ZhangTexas Therapeutics Institute, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Xiaochun ChenDepartment of Neurology, Union Hospital, and Fujian Key Laboratory of Molecular Neurology, Fujian Medical University, Fuzhou, Fujian 350001, China.
Guojun BuFujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian 361102, China; Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.
Zhiqiang AnTexas Therapeutics Institute, The Brown Foundation Institute of Molecular Medicine, University of Texas Health Science Center at Houston, Houston, TX 77030, USA.
Timothy Y HuangNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA.
Huaxi XuNeuroscience Initiative, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA 92037, USA; Fujian Provincial Key Laboratory of Neurodegenerative Disease and Aging Research, Institute of Neuroscience, College of Medicine, Xiamen University, Xiamen, Fujian 361102, China. Electronic address: xuh@sbpdiscovery.org.
Sanford Burnham Prebys Medical Discovery Institute · USBrown Foundation · USFujian Medical University · CNXiamen University · CN
Funding
Molecular pathobiology of soluble TREM2 in Alzheimer's disease.RF1AG056130 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI HUANG, TIMOTHY YIKAI, ZHAO, NA · 2017 to 2023
$6.8MRegulation of Protein Trafficking in NeurodegenerationR01NS046673 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2003 to 2018
$5.8MBAC Transgenic Mouse Models of TREM2 to Study Neuroprotective Mechanisms in ADRF1AG056114 · NIA · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI YANG, XIANGDONG WILLIAM · 2017 to 2017
$4.1MThe Role of Appoptosin in Alzheimer's Disease and Other TauopathiesR01AG038710 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2011 to 2019
$3.9MIdentifying genes in Beta-Amyloid ProductionR01AG021173 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2004 to 2015
$3.3MRoles of SN27 in regulating glutamate receptors during neurodegenerationR01AG044420 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2013 to 2017
$2.0MThe Role of DLG5 in Alzheimer's DiseaseR21AG048519 · NIA · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI XU, HUAXI · 2015 to 2016
$536kNIA NIH HHS R01 AG021173NIA NIH HHS R01 AG038710NIA NIH HHS R01 AG044420NIA NIH HHS R21 AG048519NIA NIH HHS RF1 AG056114NIA NIH HHS RF1 AG056130NINDS NIH HHS R01 NS046673
Abstract
Mutations in triggering receptor expressed on myeloid cells 2 (TREM2) have been linked to increased Alzheimer's disease (AD) risk. Neurobiological functions of TREM2 and its pathophysiological ligands remain elusive. Here we found that TREM2 directly binds to β-amyloid (Aβ) oligomers with nanomolar affinity, whereas AD-associated TREM2 mutations reduce Aβ binding. TREM2 deficiency impairs Aβ degradation in primary microglial culture and mouse brain. Aβ-induced microglial depolarization, K
Indexed as
AgedAged, 80 and overAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCells, CulturedDouble-Blind MethodFemaleHEK293 CellsHumansMaleMembrane GlycoproteinsMiceMice, Inbred C3HMice, Inbred C57BLAmyloid beta-PeptidesMembrane GlycoproteinsReceptors, ImmunologicTrem2 protein, mouseAlzheimer’s diseaseAβmicroglianeuroinflammationR47HTREM2
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